ライフサイエンスコーパス: DHEA

1 DHEA accelerated impaired healing in an impaired healing

2 DHEA action involves induction of PPARalpha mRNA and pro

3 DHEA also increased miR-21 in primary human hepatocytes

4 DHEA and androstenedione are synthesized by the adrenals

5 DHEA and testosterone appear to interact and modulate th

6 DHEA did not alter the small number (<3%) of newly forme

7 DHEA directly inhibited human and murine Th17 cells, ind

8 DHEA dosing was flexible (100-400 mg/day).

9 DHEA increased androgen receptor, c-Fos, and c-Jun recru

10 DHEA increased c-Jun, but not c-Fos, protein expression

11 DHEA increased ERK1/2 and c-Src phosphorylation in a GPE

12 DHEA induced both PPARalpha mRNA and protein levels, as

13 DHEA levels were associated with increases in cortical t

14 DHEA promoted nuclear exclusion of FoxO1 that was blocke

15 DHEA reduced memory accuracy for emotional stimuli, and

16 DHEA regulates microglial inflammatory responses through

17 DHEA replacement could play a role in prevention and tre

18 DHEA serum levels were lower in male and female MOF(1) t

19 DHEA supplementation in older women, but not in men, imp

20 DHEA treatment of endothelial cells increased PKA activi

21 DHEA was previously shown to bind to the nerve growth fa

22 DHEA, like G-1, increased GPER and ERalpha36 mRNA and pr

23 DHEA-stimulated phosphorylation of FoxO1 was inhibited b

24 DHEA-sulfate (DHEA-S), DHEA, and 17beta-estradiol stimul

25 DHEA-sulfate is associated with FEV(1)PP and is suppress

26 campal tissue (percentage conversion of [14C]DHEA to [14C]7alpha-hydroxyDHEA) was decreased selective

27 During hypoglycemia on day 2, DHEA prevented blunting of all neuroendocrine, autonomic

28 At week 26, DHEA levels remained higher in the LPV/r arm: 0.45 versu

29 as higher in women with INSR mutations after DHEA than in women with PCOS and controls (874.2 [SE 242

30 ale scores was observed in 23 subjects after DHEA and in 13 subjects after placebo treatments.

31 tions were greater (P < 0.05) in women after DHEA than after placebo.

32 Based on intention-to-treat analyses, DHEA therapy compared with placebo induced significant d

33 collected from the ADHD patients to analyze DHEA and DHEA-S levels.

34 ion is common in patients with HIV/AIDS, and DHEA appears to be a useful treatment that is superior t

35 During the protein challenge, cortisol and DHEA declined over 5 h.

36 During OGTT, cortisol and DHEA increased after the third hour and began to show si

37 did protein, and it stimulated cortisol and DHEA.

38 dy tested the hypothesis that serum DHEA and DHEA-S are predictors of major coronary heart disease (C

39 metry to analyze baseline levels of DHEA and DHEA-S in the prospective population-based Osteoporotic

40 Both DHEA and DHEA-S levels were inversely associated with the age-adj

41 d from the ADHD patients to analyze DHEA and DHEA-S levels.

42 However, mice produce DHEA and DHEA-sulfate (DHEAS) in the fetal brain.

43 precursors dehydroepiandrosterone (DHEA) and DHEA-sulfate has evolved in humans.

44 creases in brain concentrations of DHEAS and DHEA after injection of DHEAS i.p. were attenuated by pr

45 9 +/- 0.1; peak: 12.7 +/- 0.9 microg/dL) and DHEA (baseline: 15.6 +/- 1.3; nadir: 11.2 +/- 1.0; peak:

46 E2 and DHEA-S levels were strong predictors of case status (C s

47 age) is associated with both performance and DHEA levels.

48 onship between disease/fibrosis severity and DHEA-S levels was not seen in patients with cholestatic

49 Testosterone and DHEA analyses confirmed that immunocastration was an eff

50 nvolves hormone mechanisms (testosterone and DHEA) that contribute to disruption of hippocampal brain

51 Serum testosterone and DHEA-S levels were not statistically significantly assoc

52 ral conversion of the weak adrenal androgens DHEA and androstenedione into the AR ligands testosteron

53 ized gold nanoparticles (AuNPs-ARG) and anti-DHEA IgM antibodies (ox-GCE/AuNPs-ARG/IgM).

54 In the competitive affinity assay, DHEA-S specifically binds to aptamer molecules pre-hybri

55 GPER antagonist G-15 attenuated DHEA- and BSA-conjugated DHEA-stimulated pri-miR-21 tran

56 The association between DHEA and CHD risk remained significant after adjustment

57 The association between DHEA-S and severity of NAFLD persisted after adjusting f

58 ohort, we determined the association between DHEA-sulfate and percentage predicted forced expiratory

59 DHEA/-S, evidence for an association between DHEA/-S levels and cardiovascular events is contradictor

60 trated a strong positive correlation between DHEA levels and performance on digit span forward/backwa

61 n disposition indexes did not differ between DHEA- and placebo-treated women, indicating that the sli

62 There was also an interaction between DHEA and testosterone on cortical thickness of the right

63 tudies have examined the interaction between DHEA- and testosterone-related cortical maturation in hu

64 n N,N'-(1,2-dihydroxyethylene)bisacrylamide (DHEA) cross-linked pNIPMAm inner shell.

65 or (S)-orteronel were identical for blocking DHEA formation from pregnenolone and for 17alpha-hydroxy

66 Furthermore, elevated blood DHEA-S levels at 12 h after treatment in the mouse may a

67 Both DHEA and DHEA-S levels were inversely associated with th

68 Both DHEA and testosterone have been reported in animal and i

69 nt of primary rat hepatocytes decreased both DHEA- and nafenopin-induced FACO activity in primary rat

70 d sex steroid synthesis and disordered brain DHEA production and thus provide phenotypic clues about

71 ined the timescale of neuronal activation by DHEA, using light-induced release of DHEA from targeted

72 the expansion of IL-10-producing T cells by DHEA.

73 and protein were significantly increased by DHEA.

74 hat androgen precursors such as cholesterol, DHEA and progesterone, as well as androgens are highly u

75 is strongly associated with low circulating DHEA-S.

76 ist G-15 attenuated DHEA- and BSA-conjugated DHEA-stimulated pri-miR-21 transcription.

77 In contrast, DHEA/-S showed no statistically significant association

78 oncentration and a reduction in the cortisol/DHEA-ratio in hair.

79 e and after 1 yr of treatment with 50 mg/day DHEA or P.

80 A "dose effect" of decreasing DHEA-S and incremental fibrosis stage was observed with

81 ulin), hirsutism [ie, dehydroepiandosterone (DHEA) and androstenedione], and hunger (ie, ghrelin).

82 an increase in the dehydroepiandrostendione (DHEA) concentration and a reduction in the cortisol/DHEA

83 Dehydroepiandrosterone (DHEA) administration has been shown to reduce accumulati

84 Dehydroepiandrosterone (DHEA) and its sulfate, DHEAS, are the major adrenal andr

85 Dehydroepiandrosterone (DHEA) and testosterone are widely promoted as antiaging

86 Dehydroepiandrosterone (DHEA) is a neurosteroid with anxiolytic, antidepressant,

87 Dehydroepiandrosterone (DHEA) is a neurosteroid with potential effects on neurog

88 Dehydroepiandrosterone (DHEA) is a ubiquitous adrenal hormone with immunomodulat

89 Dehydroepiandrosterone (DHEA) is a weak androgen also used to elevate testostero

90 Dehydroepiandrosterone (DHEA) is an endogenous adrenal steroid hormone with cont

91 Dehydroepiandrosterone (DHEA) is the most abundant circulating steroid hormone i

92 Dehydroepiandrosterone (DHEA) is the most abundant steroid hormone and has been

93 Dehydroepiandrosterone (DHEA) regulates gene expression as a ligand for a G-prot

94 Dehydroepiandrosterone (DHEA), a 19-carbon precursor of sex steroids, is abundan

95 Dehydroepiandrosterone (DHEA), a C19 human adrenal steroid, activates peroxisome

96 ect of administering dehydroepiandrosterone (DHEA) on short-term memory.

97 ect of administering dehydroepiandrosterone (DHEA) on visual-spatial performance in postmenopausal wo

98 version from adrenal dehydroepiandrosterone (DHEA) to potent androgens and has a germline missense-en

99 dogenous S1R agonist dehydroepiandrosterone (DHEA) as an FDA-approved model drug.

100 gnenolone (PREG) and dehydroepiandrosterone (DHEA) have been reported to improve memory in aged roden

101 ine GCF cortisol and dehydroepiandrosterone (DHEA) levels.

102 of osteoporosis, and dehydroepiandrosterone (DHEA), a ubiquitous steroid precusor, are reported to be

103 By contrast, dehydroepiandrosterone (DHEA) suppressed VZ cell proliferation in males, but not

104 erone (T), 75 mg/day dehydroepiandrosterone (DHEA), or placebo (P); and 57 elderly women were studied

105 se reactions to form dehydroepiandrosterone (DHEA) and androstenedione (Andro), respectively, critica

106 ne and SULT2A1 gene, dehydroepiandrosterone (DHEA) and its sulfated form (DHEA-S), and characteristic

107 adrenal sex hormone dehydroepiandrosterone (DHEA), which is present in serum mainly as the sulfate D

108 To determine if dehydroepiandrosterone (DHEA) replacement improves insulin secretion, insulin ac

109 had a higher median dehydroepiandrosterone (DHEA) level than infants from the 3TC arm: 3.91 versus 1

110 gen and neurosteroid dehydroepiandrosterone (DHEA) is available as over-the-counter hormonal therapy

111 hat the neurosteroid dehydroepiandrosterone (DHEA), when administered preclinically, could suppress p

112 sess the efficacy of dehydroepiandrosterone (DHEA) as a potential treatment.

113 ministration of oral dehydroepiandrosterone (DHEA) during episodes of repeated hypoglycemia can preve

114 m adrenal precursors dehydroepiandrosterone (DHEA) and DHEA-sulfate has evolved in humans.

115 echnology to release dehydroepiandrosterone (DHEA), a neurosteroid that promotes neurogenesis and neu

116 reductions in serum dehydroepiandrosterone (DHEA) concentrations may be involved in bone mineral den

117 , most significantly dehydroepiandrosterone (DHEA) and to a certain degree testosterone.

118 mutations underwent dehydroepiandrosterone (DHEA) challenge; serum androgens were measured every 30

119 without derivatizaton dehyroepiandrosterone (DHEA), 17beta-estradiol (E2), testosterone (T), and thei

120 Serum levels of sulfated DHEA (DHEA-S) were measured by enzyme-linked immunosorbent ass

121 glycemic clamp (2.9 mmol/L) following either DHEA (1,600 mg) or placebo.

122 ance test before and after 2 years of either DHEA or placebo.

123 mia were randomly assigned to receive either DHEA or placebo; 90% (69 of 77) of the DHEA patients and

124 docannabinoids, docosahexanoyl ethanolamide (DHEA) and eicosapentaenoyl ethanolamide (EPEA) by activa

125 ve oxygenated docosahexaenoyl ethanolamide- (DHEA) derived products that regulated leukocyte motility

126 ous infusion of DHEA-S (30 mg/kg; ANTE EUG + DHEA-S), 3) hyperinsulinemic hypoglycemia (2.8 +/- 0.1 m

127 Our data showed that exogenous DHEA significantly downregulated IGF-1 and its receptor

128 We find DHEA to be an effective treatment for midlife-onset majo

129 r Andro production from progesterone and for DHEA from pregnenolone, indicating a distributive charac

130 tor beta by CD4(+) T cells was necessary for DHEA-mediated EAE amelioration, as well as for direct do

131 ein phosphatase 2A (PP2A) is responsible for DHEA action, and protein phosphatase 1 might be involved

132 At baseline, mean +/- SD for DHEA versus placebo groups were Schirmer I tests 4.5 +/-

133 piandrosterone (DHEA) and its sulfated form (DHEA-S), and characteristics of attention-deficit/hypera

134 Four DHEA and one placebo group patient dropped out because o

135 ion was found between elevated levels of GCF DHEA and the severity of periodontitis.

136 Higher DHEA levels (>5 ng/mL) at week 6 were associated with hi

137 rs2270112 demonstrated significantly higher DHEA-S levels than the G allele carriers.

138 In support, 7alpha-hydroxylated DHEA increases the immune response in mice with greater

139 us infusion of DHEA-S (30 mg/kg; ANTE HYPO + DHEA-S).

140 he purpose of this study was to determine if DHEA-S could preserve counterregulatory responses during

141 te-mediated cleavage of the 1,2-diol bond in DHEA produced multiresponsive core/shell microgels with

142 in all tissues and considerable increases in DHEA in male iWAT and eWAT in response to a high-fat die

143 al permissive HSD3B1(1245C) allele increases DHEA metabolism to potent androgens.

144 l interfering RNA knockdown of PKA inhibited DHEA-stimulated phosphorylation of FoxO1.

145 In year 2, all participants took open-label DHEA (50 mg/d).

146 Finally we asked whether the EGF/LIF/DHEA-responsive stem cells had an increased potential fo

147 Like DHEA, GPER agonists G-1 and fulvestrant increased pri-mi

148 ted with a reduced risk (odds ratio per 1 ln[DHEA-S], 0.1; 95% confidence interval, 0.0-0.3; P = 0.00

149 cohorts in the advanced NAFLD group had low DHEA-S levels, with the majority in the hypoadrenal rang

150 ntal fibrosis stage was observed with a mean DHEA-S of 1.03 +/- 0.05, 0.96 +/- 0.07, 0.83 +/- 0.11, 0

151 Group 3 had significantly higher mean DHEA scores compared with group 1 (P <0.05); however, th

152 ery 30 min for 4 h after ingestion of 100 mg DHEA.

153 s substantial change in the hormonal milieu, DHEA administration produced no beneficial effects on co

154 Moreover, DHEA administration enhanced serum levels of DHEA, DHEAS

155 Neither DHEA nor low-dose testosterone replacement in elderly pe

156 We report that 10 nm DHEA increases primary miR-21 (pri-miR-21) transcription

157 shallower increases of testosterone, but not DHEA, across development, which in turn predicted shallo

158 1-fold) between PAPS and raloxifene, but not DHEA.

159 erature on vascular and metabolic actions of DHEA/-S, evidence for an association between DHEA/-S lev

160 Administration of DHEA in symptomatic mice induced regulatory CD4(+) T cel

161 We suggest that exogenous application of DHEA accelerates impaired wound repair, results which ma

162 To investigate the brain basis of DHEA's impact on emotion modulation, patients were admin

163 suggest that physiological concentrations of DHEA activate a GPER intracellular signaling cascade tha

164 Conversion of DHEA locally to downstream steroid hormones leads to est

165 effects were mediated by local conversion of DHEA to estrogen, acting through the estrogen receptor,

166 f DHEA administration and the correlation of DHEA levels and performance in the placebo condition to

167 were randomly assigned to receive 50 mg/d of DHEA or matching placebo for 6 months.

168 BNN27, a C17-spiroepoxy derivative of DHEA, was shown to have antiapoptotic properties via mec

169 ential of our nanosensor in the detection of DHEA-S and other small molecules in biomedical applicati

170 free, specific and quantitative detection of DHEA-S at clinically appropriate concentrations with an

171 can be measured to achieve the detection of DHEA-S.

172 en and women showed no significant effect of DHEA on body-composition measurements.

173 hodology that did not demonstrate effects of DHEA administration on episodic and short-term memory ta

174 ent demonstrated large beneficial effects of DHEA administration on Mental Rotation, Subject-Ordered

175 However, the effects of DHEA on human or murine pathogenic immune cells, such as

176 s, could completely eliminate the effects of DHEA on stem cell proliferation.

177 tion, coupled with the documented effects of DHEA's androgenic metabolites on visual-spatial performa

178 n vitro model to characterize the effects of DHEA, prolactin, 17beta-estradiol on insulin-growth fact

179 men with low levels of the sulfated form of DHEA and bioavailable testosterone and 57 elderly women

180 vide phenotypic clues about the functions of DHEA in mouse brain development.

181 8) plus simultaneous intravenous infusion of DHEA-S (30 mg/kg; ANTE EUG + DHEA-S), 3) hyperinsulinemi

182 8) with simultaneous intravenous infusion of DHEA-S (30 mg/kg; ANTE HYPO + DHEA-S).

183 In addition, we show that local injection of DHEA accelerates impaired healing in an ageing mouse col

184 s spectrometry to analyze baseline levels of DHEA and DHEA-S in the prospective population-based Oste

185 ression analyses demonstrated that levels of DHEA and its metabolites were positively related to cogn

186 Low serum levels of DHEA and its sulfate predict an increased risk of CHD, b

187 Levels of DHEA were positively correlated with attention as measur

188 tion significantly increases serum levels of DHEA, DHEAS, testosterone and estrone and substantially

189 DHEA administration enhanced serum levels of DHEA, DHEAS, testosterone, and estrone, and regression a

190 and Visual Search tasks and serum levels of DHEA, DHEAS, testosterone, estrone, and cortisol were me

191 th advanced NAFLD had lower plasma levels of DHEA-S than patients with mild NAFLD in both the initial

192 2-16.4; P = 0.001), whereas higher levels of DHEA-S were associated with a reduced risk (odds ratio p

193 stances (P = 0.03), whereas higher levels of DHEA-S were associated with lower right atrial pressure

194 Higher levels of E2 and lower levels of DHEA-S were associated with PAH in men.

195 is associated with low circulating levels of DHEA.

196 lation, patients were administered 400 mg of DHEA (N=14) or placebo (N=15) and underwent 3T fMRI whil

197 oglycemic clamps (2.9 mmol/L) with 800 mg of DHEA or placebo administered before each clamp.

198 Precursors of DHEA such as pregnenolone or six of its major metabolite

199 ecificity of MS/MS allowed quantification of DHEA, E2, and T with 10, 10, and 5 fmol lower limits of

200 to mouse serum and tissues reveals ranges of DHEA, E2, and T and their sulfates, and tissue-specific

201 tion by DHEA, using light-induced release of DHEA from targeted DNA nanocapsules.

202 both sexes, and neither full replacement of DHEA (in elderly men and women) nor partial replacement

203 We conclude that 2 years of replacement of DHEA in elderly men and women does not improve insulin s

204 Although there have been multiple reports of DHEA's antidepressant and anxiolytic effects, no researc

205 ret the juxtaposition of the null results of DHEA administration and the correlation of DHEA levels a

206 The synthesis of DHEA and sex steroids, but not mouse glucocorticoids and

207 Six weeks of DHEA administration was associated with a significant im

208 essant medications.Intervention Six weeks of DHEA therapy, 90 mg/d for 3 weeks and 450 mg/d for 3 wee

209 Six weeks of DHEA treatment also was associated with significant impr

210 However, most studies on DHEA have been performed in rodents, and there is little

211 effects of a four week regimen of 50 mg oral DHEA on performance on the digit span, verbal span, and

212 lled crossover design in which 50 mg of oral DHEA was administered daily in the drug condition to exp

213 n inside the DNA capsule prevents photocaged DHEA from activating neurons prematurely.

214 Compared with placebo, DHEA reduced activity in the amygdala and hippocampus, e

215 n subjects and influence the ratio of plasma DHEA:DHEA-S.

216 er, we observed processivity in pregnenolone/DHEA pulse-chase experiments.

217 However, mice produce DHEA and DHEA-sulfate (DHEAS) in the fetal brain.

218 and inhibitor studies suggest that the rapid DHEA-mediated increase in miR-21 involves a G-protein-co

219 On the basis of clinicians' ratings, DHEA was superior in the intent-to-treat analysis, where

220 Among the women, 27 received DHEA and 30 received placebo.

221 Among the men, 29 received DHEA, 27 received testosterone, and 31 received placebo.

222 in the placebo group, subjects who received DHEA for 2 years had an increase in plasma levels of sul

223 Women who received DHEA had an increase in BMD at the ultradistal radius.

224 ese data provide novel evidence for relative DHEA-S deficiency in patients with histologically advanc

225 tabolism, 112 elderly subjects with relative DHEA deficiency ingested a labeled mixed meal and underw

226 females with subcutaneous pellets releasing DHEA or 17-OH pregnenolone at a constant rate failed to

227 Despite restoring DHEA sulphate concentrations to values observed in young

228 DHEA-sulfate (DHEA-S), DHEA, and 17beta-estradiol stimulated keratinocyte and f

229 cortical thickness associated with salivary DHEA and testosterone levels in a longitudinal sample of

230 The concurrent reduction of serum DHEA levels and visual-spatial performance in this popul

231 This study tested the hypothesis that serum DHEA and DHEA-S are predictors of major coronary heart d

232 However, since DHEA tended to decrease insulin action, the change over

233 These unimNPs produced a steady DHEA release in vitro for over two months at pH7.4.

234 compound and its corresponding free steroid DHEA in brain within 1 h of injection.

235 orter, Mrp4, transports the sulfated steroid DHEA-s, and sulfated bile acids interact with Mrp4 with

236 Novel derivatives of the steroid DHEA 1, a known uncompetitive inhibitor of G6PD, were de

237 ch is present in serum mainly as the sulfate DHEA-S, is the most abundant steroid hormone in human bl

238 ly increased dehydroepiandrosterone sulfate (DHEA-S) and reduced estrone levels in KC patients compar

239 enal steroid dehydroepiandrosterone sulfate (DHEA-S) has been shown in several studies to oppose cort

240 vidence that dehydroepiandrosterone sulfate (DHEA-S) is involved in an organism's response to stress

241 osensor with dehydroepiandrosterone sulfate (DHEA-S), a small-molecule steroid hormone, as the target

242 DHEA-sulfate (DHEA-S), DHEA, and 17beta-estradiol stimulated keratinoc

243 estosterone, dehydroepiandrosterone sulfate [DHEA-S], and estradiol) influence cardiovascular disease

244 levels (E2, dehydroepiandrosterone-sulfate [DHEA-S], and testosterone) are associated with PAH in me

245 Serum levels of sulfated DHEA (DHEA-S) were measured by enzyme-linked immunosorbe

246 had an increase in plasma levels of sulfated DHEA by a median of 3.4 microg per milliliter (9.2 micro

247 57 elderly women with low levels of sulfated DHEA.

248 In summary, DHEA can acutely preserve a wide range of key neuroendoc

249 We report that systemic DHEA levels are strongly associated with protection agai

250 erty in preschool, measures of testosterone, DHEA, and hippocampal volume across school age and adole

251 n to relate baseline levels of testosterone, DHEA-S, and estradiol to the incidence of CVD (coronary,

252 aloxifene, which is considerably larger than DHEA, can bind only to the unliganded (open) enzyme, whe

253 We conclude that DHEA may have acute effects to protect against hypoglyce

254 We conclude that DHEA stimulates phosphorylation of FoxO1 via PI 3-kinase

255 These results demonstrate that DHEA reduces activity in regions associated with generat

256 We demonstrate that DHEA regulates PPARalpha action by altering both the lev

257 s provide initial neuroimaging evidence that DHEA may be useful as a pharmacological intervention for

258 In the present study we hypothesized that DHEA may stimulate PI 3-kinase-dependent phosphorylation

259 Together these results indicate that DHEA oxidative metabolism produces potent novel molecule

260 Together, our data indicate that DHEA-activated TrkA signaling is a potent regulator of m

261 We previously reported that DHEA has opposing actions in endothelial cells to stimul

262 Here we show that DHEA reduces microglia-mediated inflammation in an acute

263 Here, we show that DHEA significantly increased the growth rates of human n

264 In this study, we show that DHEA suppressed peripheral responses from patients with

265 on visual-spatial performance, suggests that DHEA administration may enhance visual-spatial performan

266 This suggests that DHEA suppresses proliferation in males via a glucocortic

267 re was a significant correlation between the DHEA and LPV/r AUC levels (rho = 0.40, P = .019) and Ctr

268 gnificant differences were noted between the DHEA and placebo groups for dry eye symptoms, objective

269 the response rate was 56% (43 of 77) for the DHEA group versus 31% (21 of 68) for the placebo group.

270 the response rate was 62% (43 of 69) for the DHEA group, compared to 33% (21 of 64) for the placebo p

271 Hence, the DHEA-loaded, CTB-conjugated unimNPs represent an RGC/S1R

272 , estrone, and cortisol were measured in the DHEA and placebo conditions.

273 n the placebo drug condition, but not in the DHEA condition.

274 rformance on the visual-spatial tasks in the DHEA condition.

275 pliance with the intervention was 97% in the DHEA group and 95% in the placebo group.

276 sterone index and estradiol increased in the DHEA group only.

277 nsulin-like growth factor 1 increased in the DHEA group only.

278 ough 7 subjects met response criteria in the DHEA group, 5 met the criteria in the placebo group, and

279 +/- 0.7% after 2 y of supplementation in the DHEA group; however, in the placebo group, spine BMD was

280 ither DHEA or placebo; 90% (69 of 77) of the DHEA patients and 94% (64 of 68) of the placebo patients

281 ide prospective, empirical evidence that the DHEA-S level is increased by acute stress in healthy hum

282 acute stress in healthy humans and that the DHEA-S-cortisol ratio may index the degree to which an i

283 ssociate from P450 17A1 before conversion to DHEA.

284 aseline during year 2 after the crossover to DHEA.

285 conversion of 17alpha-hydroxypregnenolone to DHEA than toward the 17alpha-hydroxylation of pregnenolo

286 CYP7B1, an enzyme intrinsic to DHEA metabolism, was upregulated in PMD across experimen

287 an insulin sensitivity index in response to DHEA compared with placebo (+1.4 vs -0.7, P = .005).

288 stimulation of ET-1 secretion in response to DHEA may determine whether DHEA supplementation improves

289 omoter activity and secretion in response to DHEA treatment was augmented by PI 3-kinase blockade and

290 efficiently by SULT2A1 in vitro, yet unlike DHEA, raloxifene is not sulfated in vivo.

291 Microarray analysis of cortisol- versus DHEA sulfate-producing adrenal tissue demonstrated that

292 nly to the unliganded (open) enzyme, whereas DHEA binds both the open and closed forms.

293 porter gene activity in this system, whereas DHEA treatment did not.

294 on in response to DHEA may determine whether DHEA supplementation improves or worsens cardiovascular

295 The objective was to determine whether DHEA supplementation in older adults improves BMD when c

296 oratory animals, but it is not known whether DHEA decreases abdominal obesity in humans.

297 Treatment of BAEC with DHEA inhibited transactivation of the ET-1 promoter repo

298 ntrations did not differ in men treated with DHEA or placebo.

299 helial cells (BAEC and HAEC), treatment with DHEA (100 nM) acutely enhanced phosphorylation of FoxO1.

300 rapidly dephosphorylated upon treatment with DHEA and nafenopin.